Sevoflurane inhibits progression of glioma via regulating the HMMR antisense RNA 1/microRNA-7/cyclin dependent kinase 4 axis
| Autor: | Longqiu Yang, Xi'an Bao, Jun Shen, Yibo Peng |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Male
CDK4 Cell Survival sevoflurane Bioengineering Applied Microbiology and Biotechnology Mice Glioma Cell Line Tumor microRNA medicine Animals Neoplasm Invasiveness Viability assay neoplasms Messenger RNA Mice Inbred BALB C biology Cyclin-dependent kinase 4 Chemistry Cell growth Brain Neoplasms HMMR-AS1 RNA miR-7 Cyclin-Dependent Kinase 4 General Medicine medicine.disease Reverse transcription polymerase chain reaction MicroRNAs biology.protein Cancer research Disease Progression RNA Long Noncoding TP248.13-248.65 Biotechnology Research Article Research Paper |
| Zdroj: | Bioengineered article-version (VoR) Version of Record Bioengineered, Vol 12, Iss 1, Pp 7893-7906 (2021) |
| ISSN: | 2165-5987 2165-5979 |
| Popis: | Sevoflurane (Sev) is a volatile anesthetic that can inhibit tumor malignancy. Glioma is a main brain problem, but the mechanism of Sev in glioma progression is largely unclear. This study aims to explore a potential regulatory network of long noncoding RNA (lncRNA)/microRNA (miRNA)/mRNA associated with the function of Sev in glioma progression. LncRNA HMMR antisense RNA 1 (HMMR-AS1), miR-7 and cyclin-dependent kinase 4 (CDK4) abundances were examined via quantitative reverse transcription polymerase chain reaction and western blot. Cell viability, invasion, and colony formation ability were analyzed via cell counting kit-8, transwell analysis, and colony formation. The target association was analyzed via dual-luciferase reporter analysis and RNA pull-down. The in vivo function of Sev was investigated by xenograft model. HMMR-AS1 abundance was increased in glioma tissues and cells, and reduced via Sev. Sev constrained cell viability, invasion, and colony formation ability via decreasing HMMR-AS1 in glioma cells. miR-7 expression was decreased in glioma, and was targeted via HMMR-AS1. HMMR-AS1 silence restrained cell viability, invasion, and colony formation ability by up-regulating miR-7 in glioma cells. Sev increases miR-7 abundance via decreasing HMMR-AS1. CDK4 was targeted via miR-7, and highly expressed in glioma. miR-7 overexpression inhibited cell viability, invasion, and colony formation ability via reducing CDK4 in glioma cells. CDK4 expression was reduced by Sev via HMMR-AS1/miR-7 axis. Sev suppressed cell growth in glioma by regulating HMMR-AS1. Sev represses glioma cell progression by regulating HMMR-AS1/miR-7/CDK4 axis. |
| Databáze: | OpenAIRE |
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